Download The Right Ventricle During the Acute Respiratory Distress Syndrome

The Open Nuclear Medicine Journal, 2010, 2, 119-124
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The Right Ventricle During the Acute Respiratory Distress Syndrome
Revisited by Echocardiography
Vincent Caille and Antoine Vieillard-Baron*
Intensive Care Unit, University hospital Ambroise Paré, Assistance Publique des Hôpitaux de Paris, 9 avenue Charles
de Gaulle, 92104 Boulogne, France
Université de Versailles Saint Quentin en Yvelines, Faculté de Médecine Paris Ile de France Ouest, 78000 Saint
Quentin en Yvelines, France
Abstract: We illustrate the valuable information provided by echocardiography for hemodynamic monitoring and for
optimizing ventilatory strategies, during ARDS. Although the transthoracic and the transesophageal routes can be used,
we always prefer, in the absence of contraindications, to perform transesophageal echocardiography.
ARDS includes numerous affections which brutally damage the interface between the distal airway tract and pulmonary
vascular bed. Two factors combine to produce right ventricular systolic overload, the pathologic features of the syndrome
per se and mechanical ventilation.
Acute cor pulmonale (ACP) reflects the severity of the pulmonary disease, but may also be caused or exacerbated by an
aggressive and unsuitable ventilatory strategy. With tidal volume limitation, the incidence of ACP has declined to 25%.
Providing that ventilatory management is adapted to right ventricular function, ACP is no longer significantly associated
with increased mortality. If not, it is demonstrated that right ventricular dysfunction is actually associated with a poor
prognosis.
In conclusion, whereas some have promoted a lung protective approach, echocardiography allows us to promote a right
ventricular protective approach, by adapting respiratory settings to right ventricular function, which is key in the
prognosis of these patients.
Keywords: ARDS, hemodynamics, right ventricle, echocardiography.
INTRODUCTION
In recent years, bedside use of Doppler echocardiography
has supplanted invasive procedures in assessing cardiac
function in critically ill patients. Pulmonary artery
catheterization, an invasive procedure, gives indirect
information related to right-sided heart function. This
technique was gradually compromised, the measures being
of debatable reliability in mechanical ventilation [1]. A
qualitative and repetitive echocardiographic evaluation, by a
simple visualization in real time of the kinetics and size of
cardiac cavities, has been shown to be essential in assessing
right-sided heart afterloading [2]. In addition, it should be
considered that right ventricular dysfunction may affect left
ventricular function, not only by limiting left ventricular
preload, but also by adverse systolic and diastolic
interactions via the intraventricular septum and the
pericardium (ventricular interdependence). An experienced
critical care intensivist with a sufficient echocardiographic
background can immediately establish a functional diagnosis
and aid clinical decision-making. In this clinical review we
illustrate the valuable information provided by
*Address correspondence to this author at the Intensive Care Unit,
University hospital Ambroise Paré, Assistance Publique des Hôpitaux de
Paris, 9 avenue Charles de Gaulle, 92104 Boulogne, France; Tel:
+33149095603; E-mail: [email protected]
1876-388X/10
echocardiography for hemodynamic monitoring and for
optimizing ventilatory strategies, during ARDS, a situation
well known to be associated with pulmonary hypertension
and right heart dysfunction.
PHYSIOLOGY AND PATHOPHYSIOLOGY
Systolic function of the right ventricle may be
represented by the coupling between “intrinsic” contractility
of the right ventricle and its afterload [3]. In physiologic
conditions, contractility is somewhat secondary, because
simple negative pleural pressure produced by breathing
promotes blood flow through the pulmonary circulation and
ensures sufficient pulmonary venous return. The right
ventricle acts as a passive conduit. This is possible because
the right ventricle ejects blood into a low-resistance, highcompliance circuit. The volume of blood present in the
pulmonary circulation is the filling reserve of the left
ventricle. A reduction in this volume immediately affects the
left ventricular preload and may cause decreased left
ventricular stroke volume and finally circulatory failure.
Conversely, in pathologic conditions in which there is
some increase in pulmonary vascular resistance, “intrinsic”
contractility becomes essential to maintain an optimal
coupling between the right ventricle and the pulmonary
circulation and then to promote pulmonary blood flow.
Unfortunately, unlike the left ventricle, adaptation of the
2010 Bentham Open
120 The Open Nuclear Medicine Journal, 2010, Volume 2
right ventricle is limited. It can be argued that right
ventricular systolic function is sensitive: even a slight
increase in pulmonary vascular resistance can overload a
normal right ventricle, thereby impairing its systolic
function. In response, because of a significantly low diastolic
elastance, the right ventricle dilates acutely [4]. It can be
argued that right ventricular diastolic function is tolerant.
ARDS includes numerous affections which brutally
damage the interface between the distal airway tract and
pulmonary vascular be d. Two factors combine to produce
right ventricular systolic overload. The first regards the
pathologic features of the syndrome per se, which is
associated with distal occlusion of the pulmonary arterial bed
[5]
and
with
pulmonary
vascular
remodeling
(muscularization of usually non-muscularized arteries)
mediated by hypoxia and hypercapnia (Fig. 1). The second
factor is mechanical ventilation, which increases right
ventricular outflow impedance because of the elevated
transpulmonary pressure due to lung compliance impairment
[6,7]. Increasing tidal volume increases right ventricular
afterload during tidal ventilation, whereas increasing PEEP
induces increased afterload during both tidal ventilation and
expiration (Fig. 2) [8]. When right ventricular afterload is
progressively increased, the related prolonged right
ventricular contraction is responsible for a reversal in the
transseptal pressure gradient, especially at end systole [9,10].
This explains why paradoxical septal motion can be
observed.
As a consequence, pulmonary hypertension is common in
ARDS [11]. In certain situations, it can lead to a pattern of
Caille and Vieillard-Baron
acute cor pulmonale (ACP), defined as the association
between right ventricular enlargement, indicative of diastolic
overload, and paradoxical septal motion, indicative of
systolic overload (Fig. 3) [12]. The echocardiographic
pattern of ACP complicating ARDS was first described in
1985 [13].
ECHOCARDIOGRAPHIC EXAMINATION IN ARDS
Although the transthoracic and the transesophageal
routes can be used, we always prefer, in the absence of
contraindications,
to
perform
transesophageal
echocardiography. In these mechanically ventilated patients,
it is safe, minimally invasive and allows good reproducibility
of the evaluation, whoever the operator, at different periods
of time.
Echocardiographic examination of the right ventricle
requires a long-axis view of the heart to evaluate the size of
the cavity and a short-axis view to evaluate the septal
kinetics. The examination can be completed by Doppler
examination of the right ventricular ejection flow and of the
backward flow across the tricuspid valve when present.
Right Ventricular Size Assessment
Right ventricular diastolic dimensions can be obtained by
measuring right ventricular end-diastolic area in a long-axis
view obtained by a transthoracic or transesophageal route
(Fig. 3). The best way to quantify right ventricular dilatation
is to measure the ratio between the right and left ventricular
end-diastolic areas, which circumvents individual variation
Fig. (1). Lung sections in a rat exposed to 21% oxygen (panel A) and in a rat exposed to 10% oxygen for 10 days (panel B). Whereas in rat
A, pulmonary arteries were normally non-muscularized, pulmonary vascular remodeling occurred in rat B.
Echocardiography in ARDS
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121
Fig. (2). Right heart catheterization in a patient mechanically ventilated for ARDS during an increase in tidal volume from a low level (panel
A) to a high level (panel C). Increasing tidal volume was responsible during insufflation for an increase in the isovolumetric contraction
pressure (arrows) and for a decrease in pulmonary pulse. The two reflect a decrease in right ventricular stroke volume related to increased
afterload. T: tracheal pressure, E: esophageal pressure, RV: right ventricular pressure, PA: pulmonary artery pressure.
in cardiac size. In a group of normal volunteers, we reported
a mean normal ratio of 0.48 ± 0.12 [14]. We have thus
defined moderate right ventricular dilatation as a ratio
greater than 0.6 and major right ventricular dilatation as a
ratio greater than or equal to 1 [12]. However, gradation of
right ventricular dilatation by ventricular diastolic area ratio
may be inoperative when chronic left ventricular dilatation is
present, because of valvular disease or dilated
cardiomyopathy.
pulmonale, pulmonary hypertension may be lacking because
major right ventricular failure with inefficient right
ventricular contraction is responsible for markedly low
cardiac output [16].
Septal Dyskinesia
Paradoxical septal motion is best observed in a short-axis
view recorded by either a parasternal or transgastric
approach (Fig. 3). When present at end-systole, it reflects
systolic overload of the right ventricle, as emphasized above.
Most of the time, the evaluation of septal kinetics is
qualitative, but the systolic eccentricity index has been
proposed to “quantify” the systolic overload of the right
ventricle [15]. A value close to 1 is normal, whereas a value
higher than 1 reflects systolic overload of the right ventricle.
Doppler examination of pulmonary artery flow velocity
can reveal alterations of the flow due to acute pulmonary
hypertension: a decrease in the velocity time integral,
reflecting the decrease in right ventricular stroke volume, a
reduction in acceleration time and sometimes a biphasic flow
pattern (Fig. 4). Moreover, when pressure in the right atrium
exceeds that in the left atrium, the foramen ovale may open.
The detection of a patent foramen ovale requires contrast
echocardiography and has been greatly improved by
transesophageal echocardiography [17]. It can be also
diagnosed using color-flow Doppler echocardiography.
Pulmonary Arterial Hypertension
Left Ventricular Consequences of Acute Cor Pulmonale
Pulmonary hypertension is usually associated with
tricuspid regurgitation. Measurement of the maximal
velocity of tricuspid backward flow with continuous wave
Doppler allows estimation of systolic pulmonary artery
pressure. A moderate elevation is usually observed, but the
value should be viewed with caution because systolic
pulmonary artery pressure also depends on right ventricular
systolic fuction. In fact, in some extreme acute cor
Sudden right ventricular enlargement in the stiff
pericardial space causes left ventricular compression (Fig. 4).
In consequence, the normal left ventricular end-diastolic
volume is decreased in acute cor pulmonale [18]. Left
ventricular filling impairment in acute cor pulmonale results
from combined pulmonary vascular occlusion and septal
displacement [19]. This acute preload deficit often produces
or precipitates acute circulatory failure in this setting [18].
Interestingly, we have demonstrated in ARDS that the
right ventricle is able in only a few days to thicken in
response to an increase in pulmonary pressure. We described
a moderate thickness of the right ventricular free wall after 2
days of mechanical ventilation [2].
122 The Open Nuclear Medicine Journal, 2010, Volume 2
Caille and Vieillard-Baron
Fig. (3). Patient mechanically ventilated for severe ARDS. CT scan (panel A) showed severe bilateral lung injury, but also right ventricular
dilatation. Transesophageal echocardiography demonstrated a pattern of acute cor pulmonale with dilatation of the right ventricle (panel B)
and paradoxical septal motion in systole (panel C, arrow). RV: right ventricle, LV: left ventricle.
The latter produces abnormal left ventricular relaxation,
which is also evidenced by an abnormal mitral profile. The
ratio of peak velocity during early diastolic filling (E wave)
to peak velocity of the atrial systole (A wave) is inverted in
acute cor pulmonale complicating acute respiratory distress
syndrome [18].
WHY PROTECT THE RIGHT VENTRICLE IN
PATIENTS WITH ARDS, AND HOW?
When high tidal volumes were used (13 mL/kg), the
incidence of ACP was high (61%) and this was associated
with a poor prognosis [13]. In the most severe forms, with a
right ventricle bigger than the left ventricle, we have even
observed 100% mortality [13]. More recently, with tidal
volume limitation, the incidence of ACP in acute respiratory
distress syndrome has declined to 25% [18]. Providing that
ventilatory management is adapted to right ventricular
function, ACP is no longer significantly associated with
increased mortality. If not, it is clearly demonstrated that
right ventricular dysfunction is actually associated with a
poor prognosis. We showed that mortality was not different
in patients with or without ACP providing that the plateau
pressure is maintained below 27 cmH2O, whereas there was
a significant difference when plateau pressure was higher
than 27 cmH2O [20]. This was confirmed by Osman et al.
who reported in a large series that right ventricular
dysfunction was an independent parameter of mortality if
ventilatory settings are not adapted [21]. So, many
arguments underscore the need to adapt mechanical
ventilation to right ventricular function. Observation of ACP
may thus lead to suppression or limitation of the different
factors known to favor right ventricular systolic overload,
i.e. high plateau pressure, high PEEP and hypercapnia.
Plateau pressure should be re-examined and maintained
below 27 cmH2O, as explained above. PEEP should also be
limited. The mean PEEP in our unit in ARDS is 7 cmH2 O
Echocardiography in ARDS
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123
Fig. (4). Evolution of right ventricular function from admission (D2) to recovery (D14) in a patient ventilated because of severe ARDS
related to pneumonia. At day 2, plateau pressure was 22 cmH2O. Hemodynamics were normal. Echocardiography demonstrated moderate
dilatation of the right ventricle with an incipient biphasic pattern of the pulmonary flow. The right ventricular stroke volume was conserved.
At day 9, following major deterioration in respiratory mechanics (plateau pressure 29 cmH2O), echocardiography demonstrated major
dilatation of the right ventricle leading to strong restriction of the left ventricle. The pulmonary flow showed a clear biphasic pattern with a
decrease in right ventricular stroke volume. The patient was in shock and required high-dose norepinephrine infusion. Finally, at day 14,
after recovery of lung function, right ventricular function appeared normal and hemodynamics also. PP: plateau pressure, NE:
norepinephrine, RV: right ventricle, LV: left ventricle.
because we always favor oxygen transport rather than
oxygen content [22]. Intrinsic PEEP should absolutely be
avoided. It is often caused by an excessive respiratory rate,
an insidious cause of right ventricular afterloading [23].
Because PaCO2 is a well-known factor which promotes
pulmonary hypertension, the presence of ACP may induce
limitation of the hypercapnia. We recently reported very
poor tolerance in terms of right ventricular function in
ARDS patients subject to significant hypercapnia [24].
Hypercapnia must be limited first by increasing the
respiratory rate, without inducing intrinsic PEEP, and second
by removing the heat moisture exchanger and using instead a
heated humidifier [25]. If PEEP reduction does not appear
possible in the supine position without worsening
hypoxemia, prone positioning should be considered on day
3. We demonstrated that this positioning strategy in the most
severely ill patients, i.e. patients with a persistent P/F ratio
below 100 mmHg after 2 days of mechanical ventilation,
was responsible for a dramatic improvement in oxygenation
and in respiratory mechanics [26]. Interestingly, we reported
that it was also good for the right ventricle, by unloading it
[27].
Finally, in a very few situations, after adapting
respiratory settings to right ventricular function, NO
inhalation can be tested in patients with persistent shock
related to ACP.
CONCLUSION
In conclusion, in ARDS, acute cor pulmonale reflects the
severity of the pulmonary disease involving the
microvasculature, but may also be caused or exacerbated by
an aggressive and unsuitable ventilatory strategy. The classic
clinical description of acute cor pulmonale has to be revised
124 The Open Nuclear Medicine Journal, 2010, Volume 2
Caille and Vieillard-Baron
and completed by a more modern approach based on
echocardiographic changes in the size and function of the
heart. These echocardiographic findings allow us to assess
the hemodynamic consequences and prognostic implications
of acute respiratory distress syndrome. Whereas some have
promoted a lung protective approach, especially based on
high PEEP, echocardiography allows us to promote a right
ventricular protective approach, by adapting respiratory
settings to right ventricular function, which is key in the
prognosis of these patients.
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Revised: February 3, 2010
Accepted: February 3, 2010
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